The rationale behind this choice is that: (1) the 30-min time point recapitulates an early phase condition, wherein reduced BVR-A protein levels parallel IRS1 hyper-activation and impaired Akt/GSK3β axis as observed in GK rats; while (2) the 120-min time point mirrors a later phase, manifesting the development of insulin resistance characterized by reduced BVR-A protein levels, IRS1 inhibition, and the persistent impairment of Akt/GSK3β axis as observed in BVR-A−/− mice. The gene discussed is AKT1; the disease is Insulin resistance.